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العنوان
Role of polo like kinase 1 enzyme (PLK1) in hepatocellular carcinoma /
المؤلف
Yousef, Eman Hamdy Mohamed.
هيئة الاعداد
باحث / ايمان حمدى محمد يوسف
مشرف / ليلى أحمد عيسى
مشرف / مها رجب حبيب
مشرف / محمد السيد المسيرى
الموضوع
Hepatocellular carcinoma.
تاريخ النشر
2020.
عدد الصفحات
online resource (213 pages) :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الصيدلة ، علم السموم والصيدلانيات
تاريخ الإجازة
1/1/2020
مكان الإجازة
جامعة المنصورة - كلية الصيدلة - قسم الكيمياء الحيوية
الفهرس
Only 14 pages are availabe for public view

from 213

from 213

Abstract

Role of polo like kinase 1 enzyme (PLK1) in hepatocellular carcinoma.Hepatocellular carcinoma (HCC) regards a major global health problem. It is counted as the fifth most common cancer and the second most common cause of cancer-related death worldwide. It is characterized by a high incidence and a poor clinical prognosis. Unfortunately, the delayed diagnosis, the limited treatment options, and the resistance to chemotherapeutic drugs are considered obstacles for HCC treatment. Polo-like kinase 1 (PLK1) is a well-established mitotic regulator with a diverse range of biological functions continually being identified throughout the cell cycle. It has been shown that PLK1 is overexpressed in many tumor types and its expression often correlates with poor prognosis suggesting that PLK1 is capable of directly contributing to carcinogenesis.This study aimed to develop new effective treatment strategies that can be achieved by enhancing diagnosis accuracy and decreasing resistance to chemotherapeutic drugs to reduce mortality and improve survival rates. Therefore, the clinical value of using serum PLK1 as a diagnostic biomarker for HCC patients was investigated. Then, the potential outcome of combining natural products such as NOB and DG with doxorubicin (DOX) or Vola on tumor growth in vitro was studied. Also, the mechanism of these natural products was investigated.PLK1 is a promising diagnostic marker for HCC as it correlates with tumor size. HCC treatment with either DOX or Vola in combination with either NOB or DG induces a significant decrease in PLK1 level and enhancement of cell death. NOB and DG potentiate the apoptotic effect of Vola in cancer cells.